Hyponatraemia- Principles, Investigation and Management. Sirazum Choudhury Biochemistry
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1 Hyponatraemia- Principles, Investigation and Management Sirazum Choudhury Biochemistry
2 Contents Background Investigation Classification Normal Osmolality General management and SIADH Cases
3 Background Relatively common: - Estimated 15-30% prevalence in all acute admissions - Prevalence 2.48% in community with 0.97% incidence in 1985 Associated with gait disturbance, cognitive disturbance, osteoporosis and mortality - (Not causative)
4 Background Hyponatraemia: Serum sodium of less than 135mmol/L - Mild: Moderate: Severe: <125 Acute is <48 hours, Chronic is >48 hours. Reflects serum osmolality Hyponatraemia causes cell overhydration
5 Background adaptation
6 Background Pseudo hyponatraemia Lipid Normal Pseudo hyponatraemia True hyponatraemia 1L /1Kg Na 135 1L Na 125 1Kg Na 135 1L /1Kg Na 125 Osm/Kg-280 Osm/Kg-280 Osm/Kg-265
7 Background
8 Background - Symptoms Mild: - Asymptomatic - Headache, anorexia, nausea, lethargy Moderate: - Confusion, muscle cramps, weakness, confusion, ataxia Severe: - Drowsiness, coma, vomiting, brainstem herniation, seizures Rapid correction: - Cerebral pontine demyelinolysis
9 Assessment Examination Capillary refill Tissue turgor Radial pulse-?tachycardia Mucous membranes JVP Heart sound-?flow murmurs?s3 Breath sounds-?crepitations Ascites Peripheral oedema Investigations U+Es LFTs Osmolality (paired serum and urine) Urine Sodium and Potassium Thyroid function Tests 9am Cortisol CXR CT Head (?SIADH) If required: Lipid profile Protein electrophoresis Glucose
10 Normal Osmolalities - Pseudohyponatremia Hyponatraemia Normal osmolality Pseudohyponatraemia Hyperlipidaemia/ Hyperproteinaemia High levels of lipid or protein Does not contribute to osmolality Appropriate Hyperglycaemia Compensated osmolality Possibly raised osmolar gap depending on cause Corrected plasma Sodium: Sick Cell Syndrome Na/K ATP-ase dysfunction Associated with hypoxia and sepsis Normal compensated osmolality Measured Sodium conc. + Plasma glucose 4
11 Classification Hyponatraemia Low osmolality Hypovolaemic Euvolaemic Hypervolaemic Urine Na >30 Urine Na <30 Urine Na >30 Urine Na <30 Urine Na >30 Urine Na <30 Aldosterone deficiency Vomiting SIADH Hypothyroid Renal Failure Heart Failure Dieuretic excess Burns Diarrhoea Glucocorticoid deficiency Water Overload Cirrhosis Nephrotic Syndrome Salt losing nephropathy Pancreatitis Cerebral salt wasting
12 General Management- Emergencies If evidence of brain herniation: - Aim to raise Na by 5mmol/L in first hour, and then 1mmol/hr until resolution of neurological symptoms - If no resolution: aim to raise sodium to approximately 130mmol/L or by max 10mmol/L - Involve ITU - Sodium measurements 6 hourly Use Hypertonic saline - 3% saline in emergencies Reduces volume of fluid given
13 General Management- Emergencies
14 General Management Sodium change: Na (infusate)- Na(serum) TBW+1 TBW = Body weight x %Water %Water: Elderly = 50% Adults = 55% Children = 60% 513 mmol/l- 105mmol/L 80 X = 10mmol/L change (if given 1L of 3%)
15 SIADH Inappropriate secretion of ADH from posterior Pituitary or ectopic source Hyponatraemia with hypo-osmolality (<275mOsm/kg) Euvolaemia with raised urinary sodium (>20mOsm/kg) and inappropriately concentrated urine (>100mOsm/kg) Normal body response inhibited Free water should be excreted Normally urine osm should strictly be less than serum osm
16 SIADH Normal physiology ADH secreted Osmoreceptors detect high osmolality Aquaporin upregulated Increased sodium reabsorption (Aldosterone) Increased water reabsorption Concentrated urine Normalising Osmolality
17 SIAH - Pathophysiology Collecting Duct Increased water reabsorption Inappropriate ADH secretion Increased Luminal Sodium Low Plasma osmolality High urine Na (>30) High urine Osm (>100)
18 SIADH - Causes Intracranial pathology: Trauma, Tumour, Infection, Thrombosis Pulmonary: Small cell lung Ca, Mesothelioma, Abscesses, TB Malignancy: GI (pancreas and stomach), Lymphoma, Leukaemia Drugs: TCAs, SSRIs, AEDs, Vincristine, cyclophosphamide, Lithium, ecstasy Idiopathic
19 SIADH - Management If severe with symptoms Treat with 3% saline until resolution of symptoms or Na- 130mmol or increase of 10mmol/L Fluid restrict- 1 st line (unlikely to cause adverse effects) NaCl tablets + low dose furosemide 2 nd line Oral urea ( g/Kg) alternative 2 nd line Demeclocycline, then Vaptans in resistant cases??? Patients should not be given 0.9% saline
20 Hyponatraemia When to refer/admit There are no unified UK guidelines Only local guidelines and European guidelines NICE CKS indicate admission if patients: Have acute onset or severe hyponatraemia (serum sodium concentration of less than 125 mmol/l) Are symptomatic Have signs of hypovolaemia Discussion with endocrinology if patient: Has asymptomatic, moderate hyponatraemia (serum sodium concentration of mmol/l). If Addison's disease is suspected, admission or urgent referral may be required.
21 Hyponatraemia When to refer/admit Refer to an endocrinologist, the urgency depending on clinical judgement: If the cause of hyponatraemia is not clear. If SIAD or another endocrine cause is suspected. If reset osmostat syndrome or cerebral salt wasting is suspected. Refer to an appropriate specialist: If the person has hyponatraemia thought to be caused by heart failure, kidney disease, or liver disease.
22 Summary Treatment of hyponatraemia depends on classification Ensure that hyponatraemia is a true hyponatraemia Treat the underlying cause where possible If euvolaemic, fluid restrict and complete sodium screen
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